FAM150A and FAM150B are activating ligands for Anaplastic Lymphoma Kinase
- University of Gothenburg, Sweden
- Five Prime Therapeutics Inc., United States
Abstract
Aberrant activation of Anaplastic Lymphoma Kinase (ALK) has been described in a range of human cancers, including non-small cell lung cancer and neuroblastoma (Hallberg and Palmer 2013). Vertebrate ALK has been considered to be an orphan receptor and the identity of the ALK ligand(s) is a critical issue. Here we show that FAM150A and FAM150B are potent ligands for human ALK that bind to the extracellular domain of ALK and in addition to activation of wild type ALK are able to drive 'superactivation' of activated ALK mutants from neuroblastoma. In conclusion, our data show that ALK is robustly activated by the FAM150A/B ligands and provide an opportunity to develop ALK-targeted therapies in situations where ALK is overexpressed/activated or mutated in the context of the full length receptor.
Article and author information
Author details
Reviewing Editor
- Roger Davis, Howard Hughes Medical Institute & University of Massachusetts Medical School, United States
Version history
- Received: July 1, 2015
- Accepted: September 28, 2015
- Accepted Manuscript published: September 29, 2015 (version 1)
- Version of Record published: November 24, 2015 (version 2)
Copyright
© 2015, Guan et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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FAM150A and FAM150B are activating ligands for Anaplastic Lymphoma Kinase
eLife 4:e09811.
https://doi.org/10.7554/eLife.09811
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